Publication for Hmgcr and Idi1

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
mmu	Hmgcr	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	15357			[link]
mmu	Idi1	isopentenyl-diphosphate delta isomerase	319554

Pubmed ID	Priority	Text
22441164	0.98	HMGCR, IDI1, FPPS, SQLE, and LSS was significantly decreased in WY-14,643-treated vs. control mouse liver (Fig. 4D).
	0.98	HMGCR, IDI1, FPPS, SQLE, LSS, SREBP-2) and ER stress markers (e.g., Grp78, TRIB3, ATF4, CHOP, p8) is already increased in livers from embryonic day 18.5 SW/129 Pex2-/- mice compared to controls (W.J. Kovacs and P.L. Faust, unpublished results).
	0.97	HMG-CoA reductase (HMGCR), IPP isomerase (IDI1), FPP synthase (FPPS) and squalene synthase (SQS), were normal in livers of newborn SW/129 strain Pex2-/- mice compared to age-matched controls, but all enzyme activities were significantly elevated in the postnatal knockout mouse livers.
	0.97	HMGCR, FPPS, IDI1, SQS, squalene epoxidase (SQLE), lanosterol synthase (LSS), 7-dehydrocholesterol reductase (DHCR7), LDL receptor (LDLR) and Insig-1 were all significantly increased 1.6- to 4.7-fold in P0 129 Pex2-/- versus control mouse liver.
	0.96	HMGCR protein levels were increased 3-fold, and IDI1 and FPPS protein levels were elevated 4-fold and 2.4-fold, respectively, in 129 Pex2-/- liver compared to controls (Fig. 1A).
	0.94	HMGCR and IDI1, obtained by normalizing the enzyme specific activities to the enzyme protein content within each liver homogenate, was significantly decreased both in untreated and bile acid-fed postnatal SW/129 Pex2-/- mice, relative to controls.
	0.92	HMGCR, IDI1, and FPPS were decreased by ~40% (P=0.05) (supplemental Table S1), ~60% (P<0.001) (supplemental Table S2), and ~50% (P=0.06) (data not shown), respectively.
	0.67	HMGCR, IDI1).
	0.65	HMGCR and SQS were already increased 2.1-fold, and IDI1 activity was increased 1.6-fold in the liver of P0 129 Pex2-/- mice, relative to controls; the activity of FPPS was similar in the liver of control and 129 Pex2-/- mice (cf.
29237705	0.98	Hmgcr, Idi1, and Cyp51), as well as the known target gene Axin, were found to be up-regulated (Fig. 5 A).
	0.98	Hmgcr, Idi1, and Cyp51 (Fig. S3 D), whereas knocking down the expression of beta-catenin inhibited the expression of these enzymes (Fig. 5 B).
	0.98	HMGCR, IDI1, CYP51, and mouse Hmgcr (Fig. 5 C), suggesting that beta-catenin signaling directly regulates Hmgcs1, Hmgcr, Idi1, and Cyp51 transcription.
	0.97	Hmgcr, Cyp51, and Idi1 after disrupted ciliogenesis.
	0.97	Hmgcr, Idi1, and Cyp51, and overexpression of beta-catenin significantly activated these promoters in luciferase assays (Fig. S3 E).
23585733	0.98	Hmgcr, Sqle, Fdps, Idi1, and Ldlr) were all markedly down-regulated by 70%-90% (Figure 2E).
	0.98	Hmgcr, Sqle, Idi1, and Ldlr) by 10%-27% in the cerebral cortex and hypothalamus, as well as some decrease in Srebf2 mRNA (Figure 3E).
26226008	0.98	HMGCoA-R, HMGCoA-S1, IDI1, and cholesterol synthesis.
	0.97	HMGCoA-R, HMGCoA-S1, and isopentenyl-diphosphate delta isomerase 1 (IDI1).
19183246	0.98	IDI1, NSDHL and SQLE are members of the mevalonate pathway downstream of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and represent potent therapeutic targets for cholesterol-lowering agents.
21631939	0.98	Hmgcr, Pmvk, Idi1, Fdps, and Lss, were all up-regulated between 1.3 to 3.0 fold at the transcript level.
22252456	0.98	Hmgcr, Pmvk, Mvd, Fdps, Nsdhl, Idi1, Sc4mol, Cyp51, and Dhcr7).
22855714	0.98	Hmgcr, Fdft1, Dhcr24, Sqle and Idi1) and in the uptake of extracellular cholesterol (Ldlr) (Fig. 5B).
23812589	0.98	3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), squalene epoxidase (SQLE) and isopentenyl-diphosphate delta isomerase 1 (IDI-1), which were verified by real-time PCR analysis (Fig. 3d).
24391516	0.98	HMGR our analysis identified circadian cycles of protein abundance in the mouse liver for several key enzymes involved in cholesterol and bile acid synthesis such as HMG-CoA synthase 1 (HMGCS1), isopentenyl-diphosphate delta-isomerase 1 (IDI1), CYP51, CYP7A1 and CYP8B1 (Figure 6 and S4F).
28150810	0.98	Hmgcr, Idi1, Sqle, Cyp51, Msmo1, Hsd17b7, and Dhcr24) were among the genes down-regulated in XX/Sry Sertoli cells, suggesting that the down-regulation of the cholesterogenic genes was primarily the result of the decreased expression of Srebf2.
21203578	0.97	HMG-CoA reducatase (Hmgcr) and numerous genes in this pathway such as mevalonate kinase (Mvk), squalene epoxidase (Sqle), isopentenyl-diphosphate delta isomerase 1 (Idi1), and farnesyl diphosphate farnesyl transferase 1 (Fdft1).
22912762	0.97	Idi1) and NAD(P)H steroid dehydrogenase-like protein (Nsdhl)) were significantly decreased in the Mig-6d/d mice compared to Mig-6f/f mice while others (3-hydroxy-3-methylglutaryl-Coenzyme A reductase (Hmgcr)) were not.
30069000	0.97	Hmgcr, Hmgcs1, Hsd17b7, Idi1, Lss, Mvd, Mvk, Msmo1, Nsdhl, Pmvk, Sc5d, Sqle, and Tm7sf2 were significantly decreased in HFD livers.
28178673	0.96	IDI1 and HMGCR levels in both acRoots-treated and untreated LM3 cells (Figure 6L and 6M).
23139832	0.91	Hmgcr, Idi1, Fdps, Sqle, Dhcr7 and Pmvk), including Hmgcr - that is the gene encoding the rate limiting enzyme for cholesterol biosynthesis - were up-regulated at 4-wk..Upstream regulator analysis indicated that SREBF2, SREBF1, SIRT2, FOXO1, EGR2, PPARGC1B were predicted "active", whereas PPARA, CEBPE, HMGA1and WT1 were predicted "inhibit" (Table S5).
26957369	0.88	HMG-CoA reductase (HMGCR) and iospentenyl-diphosphate delta isomerase 1(IDI1).
27355629	0.81	isopentenyl-diphosphate delta isomerase (Idi1), 3-hydroxy-3-methyglutaryl-coenzyme A synthase 1 (HMG-CoA reductase, Hmgcs1), methylsterol monoxygenase 1 (Sc4mol), 3-hydroxy-3-methylglutaryl-coenzyme A reductase (Hmgcr) and squalene epoxidase (Sqle) are in the list of the most significantly downregulated genes in this analysis (Table 2).